Ridaforolimus
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| Category | Bioactive by-products |
| Catalog number | BBF-04028 |
| CAS | 572924-54-0 |
| Molecular Weight | 990.20 |
| Molecular Formula | C53H84NO14P |
| Purity | >95% by HPLC |
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Description
Ridaforolimus is a small molecule and non-prodrug analogue of the lipophilic macrolide antibiotic rapamycin with potential antitumor activity. Ridaforolimus binds to and inhibits the mammalian target of rapamycin (mTOR), which may result in cell cycle arrest and, consequently, the inhibition of tumor cell growth and proliferation. Upregulated in some tumors, mTOR is a serine/threonine kinase involved in regulating cellular proliferation, motility, and survival that is located downstream of the PI3K/Akt signaling pathway.
Specification
| Synonyms | AP23573; AP 23573; AP-23573; MK8669; MK 8669; MK-8669; Deforolimus |
| Storage | Store at -20°C |
| IUPAC Name | (1R,9S,12S,15R,16E,18R,19R,21R,23S,24E,26E,28E,30S,32S,35R)-12-[(2R)-1-[(1S,3R,4R)-4-dimethylphosphoryloxy-3-methoxycyclohexyl]propan-2-yl]-1,18-dihydroxy-19,30-dimethoxy-15,17,21,23,29,35-hexamethyl-11,36-dioxa-4-azatricyclo[30.3.1.04,9]hexatriaconta-16,24,26,28-tetraene-2,3,10,14,20-pentone |
| Canonical SMILES | CC1CCC2CC(C(=CC=CC=CC(CC(C(=O)C(C(C(=CC(C(=O)CC(OC(=O)C3CCCCN3C(=O)C(=O)C1(O2)O)C(C)CC4CCC(C(C4)OC)OP(=O)(C)C)C)C)O)OC)C)C)C)OC |
| InChI | InChI=1S/C53H84NO14P/c1-32-18-14-13-15-19-33(2)44(63-8)30-40-23-21-38(7)53(61,67-40)50(58)51(59)54-25-17-16-20-41(54)52(60)66-45(35(4)28-39-22-24-43(46(29-39)64-9)68-69(11,12)62)31-42(55)34(3)27-37(6)48(57)49(65-10)47(56)36(5)26-32/h13-15,18-19,27,32,34-36,38-41,43-46,48-49,57,61H,16-17,20-26,28-31H2,1-12H3/b15-13+,18-14-,33-19+,37-27+/t32-,34-,35-,36-,38-,39+,40+,41+,43-,44+,45+,46-,48-,49+,53-/m1/s1 |
| InChI Key | BUROJSBIWGDYCN-QHPXJTPRSA-N |
| Source | Streptomyces hygroscopicus |
Properties
| Appearance | White Solid |
| Antibiotic Activity Spectrum | neoplastics (Tumor) |
| Boiling Point | 996.16°C at 760 mmHg |
| Melting Point | 95-98°C |
| Density | 1.18 g/cm3 |
| Solubility | Soluble in ethanol, methanol, DMF, DMSO |
Reference Reading
1.Clinical efficacy of mTOR inhibitors in solid tumors: a systematic review.
Huang Z1, Wu Y2, Zhou X1, Qian J1, Zhu W1, Shu Y1, Liu P1. Future Oncol. 2015;11(11):1687-99. doi: 10.2217/fon.15.70.
The common dysregulation of the mTOR signaling pathway in tumor cells makes it a key target in oncotherapy. To better understand the effects of mTOR inhibitors, we analyzed 32 published clinical trials on solid tumors other than renal cell cancer, neuroendocrine tumors and metastatic breast cancer, for mTOR inhibitors are already approved by the US FDA to treat the three cancers. A lack of therapeutic effects was observed when mTOR inhibitors were used as a single agent. When combined with other agents, mTOR inhibitors still lacked sufficient clinical activity or just had minimal activity. More studies are required to better understand the clinically effects of mTOR inhibitors and the development of novel mTOR inhibitors is absolutely necessary.
2.Ridaforolimus improves the anti-tumor activity of dual HER2 blockade in uterine serous carcinoma in vivo models with HER2 gene amplification and PIK3CA mutation.
Hernandez SF1, Chisholm S2, Borger D3, Foster R4, Rueda BR4, Growdon WB5. Gynecol Oncol. 2016 Apr 1. pii: S0090-8258(16)30083-X. doi: 10.1016/j.ygyno.2016.03.027. [Epub ahead of print]
OBJECTIVE: Uterine serous carcinomas (USC) harbor simultaneous HER2 (ERBB2) over-expression and gain of function mutations in PIK3CA. These concurrent alterations may uncouple single agent anti-HER2 therapeutic efficacy making inhibition of the mammalian target of rapamycin (mTOR) a promising option to heighten anti-tumor response.
3.An unbiased oncology compound screen to identify novel combination strategies.
O'Neil J1, Benita Y2, Feldman I3, Chenard M4, Roberts B5, Liu Y4, Li J4, Kral A6, Lejnine S4, Loboda A4, Arthur W7, Cristescu R4, Haines BB8, Winter C9, Zhang T10, Bloecher A11, Shumway SD4. Mol Cancer Ther. 2016 Mar 16. pii: molcanther.0843.2015. [Epub ahead of print]
Combination drug therapy is a widely used paradigm for managing numerous human malignancies. In cancer treatment, additive and/or synergistic drug combinations can convert weakly efficacious monotherapies into regimens that produce robust anti-tumor activity. This can be explained in part through pathway interdependencies that are critical for cancer cell proliferation and survival. However, identification of the various interdependencies is difficult due to the complex molecular circuitry that underlies tumor development and progression. Here, we present a high-throughput platform that allows for an unbiased identification of synergistic and efficacious drug combinations. In a screen of 22,737 experiments of 583 doublet combinations in 39 diverse cancer cell lines using a 4 by 4 dosing regimen, both well-known and novel synergistic and efficacious combinations were identified. Here, we present an example of one such novel combination, a Wee1 inhibitor (AZD1775) and an mTOR inhibitor (ridaforolimus), and demonstrate that the combination potently and synergistically inhibits cancer cell growth in vitro and in vivo.
4.A Phase I Trial of Combined Ridaforolimus and MK-2206 in Patients with Advanced Malignancies.
Gupta S1, Argilés G2, Munster PN3, Hollebecque A4, Dajani O5, Cheng JD6, Wang R6, Swift A6, Tosolini A6, Piha-Paul SA7. Clin Cancer Res. 2015 Dec 1;21(23):5235-44. doi: 10.1158/1078-0432.CCR-15-0180. Epub 2015 Jul 17.
PURPOSE: The PI3K/Akt/mTOR signaling pathway is aberrantly activated in many cancers. Combining ridaforolimus, an mTOR inhibitor, with MK-2206, an Akt inhibitor, may more completely block the PI3K pathway and inhibit tumor growth.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
